scholarly journals Active Potassium Ion Transport Across the Caterpillar Midgut: I. Tissue Electrical Properties and Potassium Ion Transport Inhibition

1984 ◽  
Vol 108 (1) ◽  
pp. 273-291
Author(s):  
M. V. THOMAS ◽  
T. E. MAY

Active potassium ion transport by isolated midguts of Spodoptera littoralis and Manduca sexta caterpillars has been studied by electrical means. In contrast to previous studies, the electrical properties of the midguts remained essentially constant for several hours; this improvement probably results from use of an experimental saline that more closely resembles caterpillar haemolymph. The active transport could be abolished by anoxia and by a number of chemical agents, of which trimethyl tin chloride (effective at 10−9M) was the most potent. Some of these substances, including trimethyl tin chloride, may have been acting directly on the potassium ion transport system. The results of varying the ionic composition of the saline suggest that potassium is the only cation that can be transported at a significant rate. However, the rate of potassium ion transport is increased by the simultaneous presence of other inorganic cations. Experiments to determine the ‘reversal potential’ for the active transport pathway, by varying the potassium ion concentration, suggested that this parameter was not a constant, and thus the active transport system could not be modelled by a simple equivalent electrical circuit, although the midgut epithelium is not unique in this respect. Therefore, the tissue electrical properties could not readily be correlated with the energetics of the potassium transport process, but the results are nevertheless consistent with a potassium ion: ATP ratio of greater than one, if ATP is indeed the primary energy source.

2021 ◽  
Author(s):  
Qin Yang ◽  
Qingqing Tan ◽  
Changjun Lan ◽  
Bozhen Lv ◽  
Guimei Zhou ◽  
...  

Science ◽  
1992 ◽  
Vol 256 (5057) ◽  
pp. 663-665 ◽  
Author(s):  
H Sentenac ◽  
N Bonneaud ◽  
M Minet ◽  
F Lacroute ◽  
J. Salmon ◽  
...  

Author(s):  
G. Zampighi ◽  
M. Kreman

The plasma membranes of most animal cells contain transport proteins which function to provide passageways for the transported species across essentially impermeable lipid bilayers. The channel is a passive transport system which allows the movement of ions and low molecular weight molecules along their concentration gradients. The pump is an active transport system and can translocate cations against their natural concentration gradients. The actions and interplay of these two kinds of transport proteins control crucial cell functions such as active transport, excitability and cell communication. In this paper, we will describe and compare several features of the molecular organization of pumps and channels. As an example of an active transport system, we will discuss the structure of the sodium and potassium ion-activated triphosphatase [(Na+ +K+)-ATPase] and as an example of a passive transport system, the communicating channel of gap junctions and lens junctions.


2005 ◽  
Vol 127 (38) ◽  
pp. 13316-13323 ◽  
Author(s):  
Lucia Becucci ◽  
Maria Rosa Moncelli ◽  
Renate Naumann ◽  
Rolando Guidelli

1975 ◽  
Vol 65 (5) ◽  
pp. 599-615 ◽  
Author(s):  
L J Mandel

Increases in transepithelial solute permeability were elicited in the frog skin with external hypertonic urea, theophylline, and vasopressin (ADH). In external hypertonic urea, which is known to increase the permeability of the extracellular (paracellular) pathway, the unidirectional transepithelial fluxes of Na (passive), K, Cl, and urea increased substantially while preserving a linear relationship to each other. The same linear relationship was also observed for the passive Na and urea fluxes in regular Ringer and under stimulation with ADH or 10 mM theophylline, indicating that their permeation pathway was extracellular. A linear relationship between Cl and urea fluxes could be demonstrated if the skins were separated according to their open circuit potentials; parallel lines were obtained with increasing intercepts on the Cl axis as the open circuit potential decreased. The slopes of the Cl vs. urea lines were not different from that obtained in external hypertonic urea, indicating that this relationship described the extracellular movement of Cl. The intercept on the ordinate was interpreted as the contribution from the transcellular Cl movement. In the presence of 0.5 mM theophylline or 10 mU/ml of ADH, mainly the transcellular movement of Cl increased, whereas 10 mM theophylline caused increases in both transcellular and extracellular Cl fluxes. These and other data were interpreted in terms of a possible intracellular control of the theophylline-induced increase in extracellular fluxes. The changes in passive solute permeability were shown to be independent of active transport. The responses of the active transport system, the transcellular and paracellular pathways to theophylline and ADH could be explained in terms of the different resulting concentrations of cyclic 3'-5'-AMP produced by each of these substances in the tissue.


1988 ◽  
Vol 8 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Cesar N. Raffin ◽  
Thomas J. Sick ◽  
Myron Rosenthal

To examine the relationships between brain glycolysis, ion transport, and mitochondrial reduction/oxidation (redox) activity, extracellular potassium ion activity (K+0) and redox shifts of cytochrome oxidase (cytochrome a,a3) were recorded previous to and during superfusion of rat cerebral cortex with the glycolytic inhibitor iodoacetic acid (IAA). IAA produced oxidation of cytochrome a,a3, increased local oxygenation, increased K+0, and, in response to neuronal activation, slowed rates of K+0 reaccumulation. Rates of rereduction of cytochrome a,a3, after the oxidation of this cytochrome by stimulation, were also slowed by IAA. These effects of IAA demonstrate the dependence of K+0 reaccumulation on the integrity of glycolysis, support the concept that active processes are involved in brain ion transport, and suggest a link between ATP supplied by glycolysis and ion transport activity. These data are also compatible with the suggestion that residual dysfunctions after brain ischemia result from derangements in glycolytic functioning rather than from limitations in oxygen availability or oxidative metabolic activity.


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